Reduced fecundity, dissociable from adult worm death, occurs in several experimental schistosome infections including Schistosoma mansoni in baboons. Evidence suggests that host influences, perhaps mediated by the immune system, are responsible. If so, then fecundity is actively suppressed in these chronic infections, and new avenues for development of a vaccine against schistosomiasis would be possible. Reduced fecundity adult worms will be transplanted from chronically infected into naive baboons, in order to see if fecundity is resumed in the new host. The hypothesis that fecundity suppression is mediated immunologically will be tested both indirectly and directly. Indirect approaches include correlating anti-schisotosome antibodies measured by k-ELISA with fecundity status, searching by in vitro assays for antibodies which could influence fecundity in vivo, examining the orientation of surface-bound immunoglobulins to distinguish between antibody-specific and nonspecific activities, and studying the underlying cellular basis for formation of antibodies that may influence fecundity. Direct approaches will include 1) immunosuppression in baboons with reduced fecundity infections to test if reduced fecundity is under immunologic control, and 2) attempts to reduce fecundity or inhibit fecundity resumption in percutaneous or surgically introduced infections, respectively, by means of passively administering antibodies with demonstrated in vitro activity, or antibodies correlating well with in vivo fecundity reduction.